title: The impact of oral vitamin A derivatives on lipid metabolism - What recommendations can be derived for dealing with this issue in the daily dermatological practice?
abstract: Retinoids and vitamin A derivatives have been widely used topically and systemically in the treatment of hyper- and parakeratotic skin diseases, genodermatoses, severe acne, autoimmune diseases (i. e. lupus erythematosus) or cutaneous T-cell lymphoma for more than 30 years. In addition to the desired proliferation-inhibiting, differentiation-inducing and antiinflammatory or sebo-suppressive effects, vitamin A derivatives also affect lipid metabolism. This is shown primarily by an increase of transaminases, triglycerides or cholesterol levels which vary in intensity from patient to patient. The degree of impact on the different parameters of lipid metabolism depends on the nature of the vitamin A derivative on the one hand due to different receptor specific binding interactions (RAR/RXR), while on the other hand posttranslational processes also play a major role. This review paper gives a brief, concise overview of the vitamin A derivatives and possible effects on lipid metabolism that can be expected. Additionally it contains a recommendation for secure handling of abnormal laboratory values before, during and after oral therapy with vitamin A derivatives. The aim of this article is to provide practical help and confidence in dealing with vitamin A derivatives in daily clinical practice. The publication was created in cooperation with the Deutsche Dermatologische Gesellschaft (DDG) and Deutsche Gesellschaft zur Bekämpfung von Fettstoffwechselstörungen und ihren Folgeerkrankungen (DGFF [Lipid-Liga] e. V.).
authors.affiliation: Department of Endocrinology, Diabetology, Metabolism and Nutritional Medicine, University Clinic of Giessen and Marburg, Germany.
authors.forename: Hans-Ulrich
authors.initials: HU
authors.lastname: Klör
authors.forename: Achim
authors.initials: A
authors.lastname: Weizel
authors.forename: Matthias
authors.initials: M
authors.lastname: Augustin
authors.forename: Thomas L
authors.initials: TL
authors.lastname: Diepgen
authors.forename: Peter
authors.initials: P
authors.lastname: Elsner
authors.forename: Bernhard
authors.initials: B
authors.lastname: Homey
authors.forename: Alexander
authors.initials: A
authors.lastname: Kapp
authors.forename: Thomas
authors.initials: T
authors.lastname: Ruzicka
authors.forename: Thomas
authors.initials: T
authors.lastname: Luger
mesh_terms: D000284:Administration, Oral; D050197:Atherosclerosis / Q000097:blood / Q000139:chemically induced* / Q000235:genetics*; D016903:Drug Monitoring; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000139:chemically induced* / Q000235:genetics*; D015228:Hypertriglyceridemia / Q000097:blood / Q000139:chemically induced* / Q000235:genetics*; D050356:Lipid Metabolism / Q000187:drug effects* / Q000235:genetics; D008055:Lipids / Q000097:blood; D012176:Retinoids / Q000008:administration & dosage* / Q000009:adverse effects; D012307:Risk Factors; D012871:Skin Diseases / Q000188:drug therapy*; D014801:Vitamin A / Q000008:administration & dosage* / Q000009:adverse effects / Q000031:analogs & derivatives*
chemical_list: D008055:Lipids; D012176:Retinoids; D014801:Vitamin A